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Biomedical subjects

T Kanno

Publications and source records attributed to T Kanno.

At least 109 records · Page 6Linked to original sources
PubMed2000

Corrosion resistance of the Pt-Fe-Nb magnets for dental-casting.

Magnetic attachments have been used in clinical dental practice, but there is some difficulties associated with removable bridges. One possible solution is to make whole bridges of Pt-Fe magnet alloys and its abutment out of magnetic stainless steel by casting. In terms of castability and magnetic properties, the promising composition of the Pt-Fe-Nb magnet alloy is Pt-30.0 mass% Fe-0.6 mass% Nb and Pt-30.0 mass% Fe-0.5 mass% Nb-0.03 mass% Si. In the present study, the corrosion resistance of these alloys was investigated based on the elusion test, electrochemical behavior and surface characterization by EPMA analysis. The released elements from the Pt-Fe-Nb magnets were mainly Fe ions in quantities similar to that of stainless steel for biomedical use, and the Pt-Fe-Nb magnet alloy, the Pt-Fe-Nb-Si magnet alloy and platinum resembled each other in electrochemical behavior. The present findings suggest, that the Pt-Fe-Nb magnet alloy provides excellent corrosion resistance and has important clinical dental applications.

Analysis of Variance↗
PubMed2000

Protein kinase C-dependent inhibition of K+ currents in noradrenaline-induced depolarization of smooth muscle of guinea-pig vas deferens.

Ionic mechanisms and signal transduction underlying noradrenaline (NA)-induced depolarization in single smooth muscle cells of guinea-pig vas deferens were studied. NA caused depolarization followed by action potentials through activation of 1-adrenoceptors. In the presence of nifedipine, no action potential was generated, and the magnitude of the depolarization depended on the concentration of NA (0.1-100 micrometer). NA, through 1-adrenoceptor activation, reduced the magnitude of membrane currents in response to voltage ramp pulses from -90 to -30 mV in a concentration-dependent manner. The reversal potential of the current inhibited by NA changed proportionally to the change in the equilibrium potential of K+, suggesting that NA inhibited K+ channel activity. Treatment of cells with GDPS, an inhibitor of G proteins, or bisindolylmaleimide (BIM), a selective protein kinase C (PKC) inhibitor, prevented the NA inhibition of the currents. Application of 12-O-tetradecanoylphorbol 13-acetate (TPA), an activator of PKC, mimicked the effect of NA. It is suggested that in the smooth muscle of guinea-pig vas deferens, activation of 1-adrenoceptors and the subsequent activation of PKC led to inhibition of K+ currents, which is responsible for the depolarization induced by NA.

Adrenergic alpha-Agonists↗
PubMed2000

[Dawning of laboratory automation; individually constructed automated systems].

In the early stages of laboratory automation, the first step toward automation was the use of a spectrophotometer equipped with a flow cell system. Then, automated machines were introduced. Furthermore, computing systems, which are necessary for automated machine systems, contributed to advances in laboratory automation. Under these primitive conditions, we devised a data processing system for clinical biochemistry and further advanced the first stage of automated laboratory system. These automated systems have gradually matured in to a total laboratory automation system. As described in this report, we designed and developed an automated system in our laboratory.

Automation↗
PubMed2000

[Investigative application of a laboratory database].

An end user computing system (EUC) is usually part of the laboratory information system. Effective use of this EUC system is described in this article. The first application of this system is for monitoring the turn-around time (TAT) of laboratory work flow. Precise time sequential data were analyzed using this end user computing system. Weekly fluctuations of TAT depended on the cyclic changes in requisition numbers of test samples. Another application of EUC was phenotype screening of genetic abnormalities. Screenings from high triglyceride and low HDL cholesterol were effective for the phenotype screening for genetic lipoprotein lipase abnormalities, and phenotype screening from high albumin cholinesterase ratio was effective for genetic abnormalities causing silent cholinesterase. Investigational application of EUC was demonstrated in two areas of laboratory research.

Cholinesterases↗
PubMed2000

[Overlap syndrome].

Explore the source record for details and available documents.

Amino Acyl-tRNA Synthetases↗
PubMed2000

Cholecystokinin analog JMV-180-induced intracellular calcium oscillations are mediated by inositol 1,4,5-trisphosphate in rat pancreatic acini.

AIM: To investigate whether inositol 1,4,5-trisphosphate (IP3) is involved in secretory response of pancreatic acini to cholecystokinin (CCK) analog Boc-Tyr (SO3H)-Nle-Gly-Trp-Nle-Asp-2-phenylethylester.2NH3 (JMV-180). METHODS: Dynamics of cytosolic Ca2+ concentration, [Ca2+]c, was recorded by ratiometry of Fura-2 in pancreatic acini. RESULTS: In perfused preparations of isolated rat pancreatic acinar cells, 2-aminoethoxydiphenylborate (2APB), a new membrane permeant inhibitory modulator of IP3-mediated calcium release from internal stores, inhibited JMV-180-induced [Ca2+]c spikes, and 2APB at 100 mumol.L-1 resulted in an immediate, complete inhibition of the spikes. CONCLUSION: Recurrent [Ca2+]c spikes induced by continuous stimulation with JMV-180 are initiated via IP3-mediated Ca2+ release from internal Ca2+ stores.

Animals↗
PubMed1999

Selective inhibition of formyl-methionyl-leucyl-phenylalanine (fMLF)-dependent superoxide generation in neutrophils by pravastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase.

It has been shown previously that inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, such as compactin, lovastatin, and pravastatin, block cholesterol synthesis, suppress lymphocyte functions, and beneficially affect atherogenesis. Recently, it was reported that compactin and lovastatin inhibit the respiratory burst of DMSO-differentiated HL-60 cells, an effect reversed by mevalonic acid. The mode of action of these inhibitors in this role is not understood fully. Thus, we studied the mechanism of inhibition of neutrophil superoxide (O2*-) generation by pravastatin and found that pravastatin at 0.5 mM inhibited the receptor-mediated tyrosine kinase (TK)-dependent pathway of O2*- generation and also luminol chemiluminescence but not the protein kinase C (PKC)-dependent or the TK- and PKC-independent pathways of O2*- generation in neutrophils. Pravastatin also inhibited the tumor necrosis factor-alpha- and formyl-methionyl-leucyl-phenylalanine-induced phosphorylation of a tyrosine of a 115-kDa protein. These effects were not reversed by mevalonate. From these results it is concluded that pravastatin inhibited receptor-mediated O2*-generation by decreasing tyrosine phosphorylation but not by inhibiting the formation of an intermediate in the biosynthesis of cholesterol.

Drug Interactions↗
PubMed1999

Voltage-gated and resting membrane currents recorded from B-cells in intact mouse pancreatic islets.

1. The perforated patch whole-cell configuration of the patch-clamp technique was applied to superficial cells in intact pancreatic islets. Immunostaining in combination with confocal microscopy revealed that the superficial cells consisted of 35 % insulin-secreting B-cells and 65 % non-B-cells (A- and D-cells). 2. Two types of cell, with distinct electrophysiological properties, could be functionally identified. One of these generated oscillatory electrical activity when the islet was exposed to 10 mM glucose and had the electrophysiological characteristics of isolated B-cells maintained in tissue culture. 3. The Ca2+ current recorded from B-cells in situ was 80 % larger than that of isolated B-cells. It exhibited significant (70 %) inactivation during 100 ms depolarisations. The inactivation was voltage dependent and particularly prominent during depolarisations evoking the largest Ca2+ currents. 4. Voltage-dependent K+ currents were observed during depolarisations to membrane potentials above -20 mV. These currents inactivated little during a 200 ms depolarisation and were unaffected by varying the holding potential between -90 and -30 mV. 5. The maximum resting conductance in the absence of glucose, which reflects the conductance of ATP-regulated K+ (KATP) channels, amounted to approximately 4 nS. Glucose produced a concentration-dependent reduction of KATP channel conductance with half-maximal inhibition observed with 5 mM glucose. 6. Combining voltage- and current-clamp recording allowed the estimation of the gap junction conductance between different B-cells. These experiments indicated that the input conductance of the B-cell at stimulatory glucose concentrations ( approximately 1 nS) is almost entirely accounted for by coupling to neighbouring B-cells.

ATP-Binding Cassette Transporters↗
PubMed1999

The novel neuropeptide Y Y(1) receptor antagonist J-104870: a potent feeding suppressant with oral bioavailability.

Neuropeptide Y (NPY) is known to induce robust feeding through the action of NPY receptors in the hypothalamus. Among the subtypes of NPY receptors, Y(1) receptors may play a key role in feeding regulation. In the present study, we demonstrated that a novel Y(1) antagonist, J-104870, shows high selectivity and potency for the Y(1) receptor with an anorexigenic effect on NPY-mediated feeding. J-104870 displaced [(125)I]peptide YY (PYY) binding to cloned human and rat Y(1) receptors with K(i) values of 0.29 and 0.54 nM, respectively, and inhibited the NPY (10 nM)-induced increase in intracellular calcium levels (IC(50) = 3.2 nM) in cells expressing human Y(1) receptors. In contrast, J-104870 showed low affinities for human Y(2) (K(i) > 10 microM), Y(4) (K(i) > 10 microM), and Y(5) receptors (K(i) = 6 microM). In rat hypothalamic membranes, J-104870 also completely displaced the binding of [(125)I]1229U91, which is known to bind to the typical Y(1) receptor, with a high affinity (K(i) = 2.0 nM). Intracerebroventricular (ICV) injection of J-104870 (200 microg) significantly suppressed NPY (5 microg)-induced feeding in satiated Sprague-Dawley rats by 74%. Furthermore, ICV and oral administration of J-104870 (200 microg and 100 mg/kg, respectively) significantly suppressed spontaneous food intake in Zucker fatty rats. These findings suggested that J-104870 is a selective and potent nonpeptide Y(1) antagonist with oral bioavailability and brain penetrability. In addition, the anorexigenic effect of J-104870 clearly revealed the participation of the Y(1) receptor in NPY-mediated feeding regulation. The potent and orally active Y(1) antagonist J-104970 is a useful tool for elucidating the physiological roles of NPY in obesity.

Administration, Oral↗
PubMed1999

Improved liquid chromatographic separation of different proteins by designing functional surfaces of cattle bone-originated apatite.

Spherical particles of cattle bone-originated hydroxyapatite (r-HAp) were prepared by dissolution-precipitation, spray-drying using a two fluid-nozzle apparatus, and subsequent heat treatment. The product had effective pore structures for liquid chromatographic separation of albumin, myoglobin, ribonuclease, lysozyme and cytochrome c. The activated surfaces of the r-HAp particles were easily prepared with desired proportions of P- and C-sites and appropriate acid-basic strength for selective protein adsorption by optimizing the synthesis conditions. Liquid chromatography columns packed with the particles exhibited high resolution and durability in protein separation, reflecting stable distribution of pore size.

Animals↗
PubMed1999

Interaction and functional cooperation of PEBP2/CBF with Smads. Synergistic induction of the immunoglobulin germline Calpha promoter.

Smads are signal transducers for members of the transforming growth factor-beta (TGF-beta) superfamily. Upon ligand stimulation, receptor-regulated Smads (R-Smads) are phosphorylated by serine/threonine kinase receptors, form complexes with common-partner Smad, and translocate into the nucleus, where they regulate the transcription of target genes together with other transcription factors. Polyomavirus enhancer binding protein 2/core binding factor (PEBP2/CBF) is a transcription factor complex composed of alpha and beta subunits. The alpha subunits of PEBP2/CBF, which contain the highly conserved Runt domain, play essential roles in hematopoiesis and osteogenesis. Here we show that three mammalian alpha subunits of PEBP2/CBF form complexes with R-Smads that act in TGF-beta/activin pathways as well as those acting in bone morphogenetic protein (BMP) pathways. Among them, PEBP2alphaC/CBFA3/AML2 forms a complex with Smad3 and stimulates transcription of the germline Ig Calpha promoter in a cooperative manner, for which binding of both factors to their specific binding sites is essential. PEBP2 may thus be a nuclear target of TGF-beta/BMP signaling.

Activin Receptors, Type I↗
PubMed1999

Exogenous microglia enter the brain and migrate into ischaemic hippocampal lesions.

We compared migration of systemically injected microglia into normal brain vs. ischaemic brain using a model of ischaemic hippocampal lesion. Microglia were labeled by a fluorescent dye using our standard phagocytosis procedure of microscopic particles and then injected intra-arterially into Mongolian gerbils subjected to ischaemia reperfusion neuronal injury. Delayed death of pyramidal neurons was confirmed by conventional histological analysis and dUTP nick end labeling (TUNEL) method. Clusters of dye-tagged cells migrating into the hippocampal ischaemic lesions were confirmed histochemically to be microglia. Since peripherally injected microglia exhibit specific affinity for ischaemic brain lesions and does not exacerbate ischaemic neuronal injury in the present model, we suggest that microglia may have a potential to be used as a piggy-back ride to deliver therapeutic genes and/or drugs for CNS repair following transitory global ischaemic insult.

Animals↗
PubMed1999

Synergy of PEBP2/CBF with mi transcription factor (MITF) for transactivation of mouse mast cell protease 6 gene.

The mi locus encodes a member of the basic - helix - loop - helix - leucine zipper (bHLH-Zip) protein family of transcription factors (hereafter called MITF). Although the bHLH-Zip family transcription factors generally recognize and bind CANNTG motifs, the expression of mouse mast cell protease 6 (MMCP-6) gene is regulated by MITF through the GACCTG motif in the promoter region. The GACCTG motif was partly overlapped the TGTGGTC sequence, which was bound by polyomavirus enhancer binding protein 2 (PEBP2). In the present study, the effect of PEBP2 on the expression of MMCP-6 gene was examined. PEBP2 that is composed of alpha and beta subunits was expressed by mast cell lines and cultured mast cells derived from spleen. The overexpression of dominant negative PEBP2 cDNA reduced the expression of MMCP-6. Moreover, the simultaneous transfection of the plasmid containing MITF cDNA and the plasmid containing PEBP2 cDNA increased the MMCP-6 promoter activity. For the synergistic action of PEBP2 and MITF, the intact GACCTG and TGTGGTC motifs were prerequisite. The PEBP2alphaB1 mutant which lacked the region downstream from the Runt domain did not bind MITF and lost the synergistic function. These results indicated that PEBP2 and MITF synergistically transactivated the MMCP-6 gene and that the region downstream from the Runt domain of PEBP2alphaB1 was essential for the physical and functional interactions with MITF.

Animals↗
PubMed1999

Estimation of the gene frequency of aceruloplasminemia in Japan.

Aceruloplasminemia is a newly recognized autosomal recessive disorder of iron metabolism that causes neurodegeneration of the retina and basal ganglia as well as diabetes mellitus. We screened the serum ceruloplasmin concentrations of 4,990 healthy adult individuals. Subsequent sequence determination of the mutant alleles showed three mutations (5-bp insertion in exon 7, one heterozygote, one-bp deletion in exon 14, two heterozygotes, nonsense mutation in exon 15, one homozygote and two heterozygotes). The gene frequency was 70/100,000. In Japan, the incidence of aceruloplasminemia was estimated to be approximately 1 per 2,000,000 in the case of nonconsanguineous marriages.

Adult↗
PubMed1999

Identification of the region of mi transcription factor which is responsible for the synergy with PEBP2/CBF.

The mi locus encodes the mi transcription factor (MITF), a member of the basic-helix-loop-helix-leucine zipper protein family of transcription factors. MITF binds the alphaB1/AML1 subtype of the alpha subunit of the polyomavirus enhancer binding protein 2 (PEBP2). These two transcription factors synergistically transactivate the mouse mast cell protease 6 (MMCP-6) gene. The interaction of PEBP2 with MITF is mediated through the region carboxy-terminal to the DNA-binding Runt domain. In the present study, we examined the region of MITF that is responsible for the interaction with PEBP2. The MITF mutant that lacked the region aa 67-152 did not bind PEBP2, and the mutant that lacked the region aa 1-152 lost the synergistic function in the transactivation of the MMCP-6 promoter. We conclude that the region amino-terminal to the basic region of MITF is required for physical and functional interactions with PEBP2.

Animals↗
PubMed1999

Acute oxidative stress modulates secretion and repetitive Ca2+ spiking in rat exocrine pancreas.

The effects of the oxidant tert-butylhydroperoxide (t-buOOH) on carbachol-stimulated pancreatic secretion in the vascularly perfused rat pancreas have been studied in parallel with [Ca2+]i signalling and amylase output in perifused rat pancreatic acinar cells. Perfusion of the pancreas with t-buOOH (0.1-1 mM) caused a rapid and irreversible inhibition of carbachol-stimulated (3x10-7 M) amylase and fluid secretion. Pre-perfusion of the pancreas with vitamin C and dithiothreitol or a cocktail of GSH and GSH-precursor amino acids provided only marginal protection against the deleterious effects of t-buOOH, even though GSH levels were elevated significantly. In perifused pancreatic acini, repetitive [Ca2+]i spikes evoked by carbachol (3x10-7 M) were sustained for 40 min. t-buOOH (1 mM) acutely increased the amplitude and duration of Ca2+ spikes, then attenuated Ca2+ spiking and subsequently caused a marked and sustained rise in [Ca2+]i. t-buOOH-induced alterations in carbachol-stimulated [Ca2+]i signalling and amylase release in perifused pancreatic acini were prevented by vitamin C. Although vitamin C restored impaired Ca2+ signalling and maintained amylase output in pancreatic acini, it seems likely that oxidative stress inhibits fluid secretion irreversibly in the intact pancreas, resulting in a loss of amylase output. Thus, perturbations in [Ca2+]i signalling may not fully explain the secretory block caused by oxidative stress in acute pancreatitis.

Amylases↗